The same studies also determined that tumors treated with PD-1/PD-L1-monoclonal antibodies (mAbs) endowed with blocking properties developed resistance through the metabolic upregulation of CD38, akin to that induced by all-trans retinoic acid (ATRA) and interferon-β in the TME (as in non-small cell lung cancer, NSCLC). The gene discussed is CD274; the disease is non-small cell lung carcinoma.